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PubMedDate not supplied

Genotoxicity assay of oil dispersants in bacteria (mutation, differential lethality, SOS DNA-repair) and yeast (mitotic crossing-over).

5 oil dispersants and a sample of paraffin were devoid of mutagenic activity in the Ames reversion test, with and without S9 mix, using 7 his- S. typhimurium strains (TA1535, TA1537, TA1538, TA97, TA98, TA100, TA102). However, 3 dispersants produced direct DNA damage in E. coli WP2, which was not repairable in repair-deficient strains (WP2uvrA, CM871, TM1080), as shown by two different DNA-repair test procedures. The uvrA excision-repair system was in all cases the most important mechanism involved in repairing the DNA damage produced by oil dispersants, while the combination of uvrA with other genetic defects (polA, recA, lexA) decreased the efficiency of the system. The observed genotoxic effects were considerably lowered in the presence of S9 mix containing liver S9 fractions from Aroclor-treated rats. The sample of oil dispersant yielding the most pronounced DNA damage in repair-deficient E. coli failed to induce gene sfiA in E. coli (strain PQ37), using the SOS chromotest, or mitotic crossing-over in Saccharomyces cerevisiae (strain D5). The direct toxicity of the oil dispersant to both bacterial and yeast cells was markedly decreased in the presence of rat-liver preparations. These two short-term tests were effective in detecting the genotoxicity of both direct-acting compounds (such as 4-nitroquinoline N-oxide and methyl methanesulfonate) and procarcinogens (such as cyclophosphamide, 2-aminoanthracene and 2-aminofluorene). Moreover, the SOS chromotest was successfully applied to discriminate the activity of chromium compounds as related to their valence (i.e. Cr(VI) genotoxic and Cr(III) inactive). Combination of oil dispersants with Cr(VI) compounds did not affect the direct mutagenicity to S. typhimurium (TA102) of a soluble salt (sodium dichromate) nor did it result in any release of a water-soluble salt (lead chromate), as also confirmed by analytical methods. On the other hand, exposure to sunlight tended to decrease, to a slow rate, the direct genotoxicity of an oil dispersant in the bacterial DNA-repair test.

Chromates↗
PubMed1998

Lung cancer mortality in nickel/chromium platers, 1946-95.

OBJECTIVES: To investigate mortality from lung cancer in nickel/chromium platers. METHODS: The mortality experience of a cohort of 1762 chrome workers (812 men, 950 women) from a large electroplating and light engineering plant in the Midlands, United Kingdom, was investigated for the period 1946-95. All subjects were first employed in chrome work at the plant during the period 1946-75, and had at least six months employment in jobs associated with exposure to chromic acid mist (hexavalent chromium). Detailed job histories were abstracted from original company personnel records and individual cumulative durations of employment in three types of chrome work were derived as time dependent variables (chrome bath work, other chrome work, any chrome work). Two analytical approaches were used--indirect standardisation and Poisson regression. RESULTS: Based on mortalities for the general population of England and Wales, male workers with some period of chrome bath work had higher lung cancer mortalities (observed deaths 40, expected deaths 25.41, standardised mortality ratio (SMR) 157, 95% confidence interval (95% CI) 113 to 214, p < 0.01) than did other male chrome workers (observed 9, expected 13.70, SMR 66, 95% CI 30 to 125). Similar findings were shown for female workers (chrome bath workers: observed 15, expected 8.57, SMR 175, 95% CI 98 to 289, p = 0.06; other chrome workers: observed 1, expected 4.37, SMR 23, 95% CI 1 to 127). Poisson regression was used to investigate risks of lung cancer relative to four categories of cumulative duration of chrome bath work and four categories of cumulative duration of other chrome work (none, < 1 y, 1-4 y, > or = 5 y). After adjusting for sex, age, calendar period, year of starting chrome work, period from first chrome work, and employment status (still employed v left employment), there was a significant positive trend (p < 0.05) between duration of chrome bath work and risks of mortality for lung cancer. Relative to a risk of unity for those chrome workers without any period of chrome bath work, risks were 2.83 (95% CI 1.47 to 5.45), 1.61 (95% CI 0.75 to 3.44), and 4.25 (95% CI 1.83 to 9.87) for the second, third, and fourth exposure categories, respectively. Duration of other chrome work was not a useful predictor of risks of lung cancer. Similar findings for both variables were obtained when adjustment was made for sex and age only. Similar findings for both variables were obtained relative to risk of chrome nasal ulceration. CONCLUSIONS: The findings are consistent with the hypothesis that soluble hexavalent chromium compounds are potent human lung carcinogens.

Adult↗
PubMed1992

Lack of renal changes in stainless steel welders exposed to chromium and nickel.

Biochemical markers of kidney damage were examined in 52 male stainless steel welders (manual metal arc welding) exposed to chromium and nickel. No difference was found in the mean urinary excretion of total proteins, albumin, protein 1, transferrin, retinol-binding protein, lactate dehydrogenase, lysozyme, or beta-N-acetylglucosaminidase in a comparison with matched referents. Beta 2-microglobulin was slightly increased in those welders with a urinary chromium concentration of greater than 64.5 nmol.mmol-1 creatinine. The prevalences of abnormal values did not differ from those observed in the reference group. No correlation was found between the concentrations of chromium or nickel in urine and that of proteins or enzymes. No consistent or clinically significant renal impairment was revealed among the stainless steel welders exposed to a chromium air concentration slightly above the current threshold limit value of the American Conference of Governmental Industrial Hygienists for water-soluble hexavalent chromium compounds (50 micrograms.m-3).

Acute Kidney Injury↗
PubMed2004

Two possible pathways for the release of arsenic during pyrolysis of chromated copper arsenate (CCA)-treated wood.

The behavior of arsenic during pyrolysis at temperatures between 135 and 500 degrees C has been widely studied. We examined the release of arsenic during the pyrolysis of chromated copper arsenate (CCA)-treated wood, and here we propose two models for the volatilization of arsenic: (a) a reacted arsenic compound, chromium arsenate, in CCA-treated wood was initially decomposed to arsenic pentoxide, which then appeared to be released at around 400-500 degrees C as a form of arsenic trioxide; and (b) an unreacted arsenic compound, arsenic pentoxide, in CCA-treated wood was released at much lower temperatures than reacted arsenic compound, as a form of arsenic trioxide. In order to restrain the release of arsenic during pyrolysis, it is possible to pyrolyze CCA-treated wood carefully at temperatures around 300-350 degrees C only if the wood contains little unreacted arsenic compound. Under these conditions, almost all toxic elements remain in the pyrolysis residue, and a weight reduction of the wood of approximately 50% can be obtained. On the other hand, the release of arsenic can be achieved easily using an unreacted arsenic compound under the same pyrolysis conditions. However, in the present study it was difficult to determine the accurate release point of arsenic in both cases due to the level of experimental uncertainty.

Arsenic↗
PubMedDate not supplied

Quantitative determination of chromium and nickel in tumour and tumour-free human tissue.

Environmental pollution with carcinogenic substances, in addition to individual abuse, are discussed as important factors causing development of cancer. We must assume that certain nickel and chromium compounds, which are ubiquitous in our ecosystem, must have carcinogenic effects on humans too. The aim of this study is therefore to examine the extent to which the accumulation of the potentially carcinogenic metal ions nickel and chromium could be measured in tissue from tumour patients. We examined tumour and tumour-free tissue obtained from a total of 48 patients who had carcinomas of the stomach, bowel, or kidney. We also analyzed nickel and chromium content in whole blood and urine samples from these persons. The quantitative metal estimations were done using atomic absorption spectrophotometry. Differences between chromium and/or nickel content in tumour or tumour-free tissue were not observed. An accumulation of these metal ions in tumour tissue is therefore improbable. We were also unable to find differences in metal content with regard to chromium and nickel as related to the appearance of tumour in the organ. In contrast, tumour patients had a 5- to 7-fold increase over normal values for chromium and nickel in blood and urine. This was attributable to unavoidable contamination of tissue and body fluids with chromium- and nickel-containing instruments during major surgical procedures.

Adult↗
PubMedDate not supplied

Workplace carcinogen and pesticide exposures in Costa Rica.

The CAREX data system converts national workforce volumes and proportions of workers exposed to workplace carcinogens into numbers of exposed in 55 industrial categories. CAREX was adapted for Costa Rica for 27 carcinogens and seven groups of pesticides. Widespread workplace carcinogens in the 1.3 million workforce of Costa Rica are solar radiation (333,000 workers), diesel engine exhaust (278,000), environmental tobacco smoke (71,000), hexavalent chromium compounds (55,000), benzene (52,000), wood dust (32,000), silica dust (27,000), lead and inorganic lead compounds (19,000), and polycyclic aromatic compounds (17,000). The most ubiquitous pesticides were paraquat and diquat (175,000), mancozeb, maneb, and zineb (49,000), chlorothalonil (38,000), benomyl (19,000), and chlorophenoxy herbicides (11,000). Among women, formaldehyde, radon, and methylene chloride overrode pesticides, chromium, wood dust, and silica dust in numbers of exposed. High-risk sectors included agriculture, construction, personal and household services, land and water transport and allied services, pottery and similar industries, woodworks, mining, forestry and logging, fishing, manufacturing of electrical machinery, and bar and restaurant personnel.

Carcinogens↗
PubMed1984

Detoxification of genotoxic compounds as a threshold mechanism limiting their carcinogenicity.

In vitro metabolic trends were assessed for 100 genotoxic agents detected in two bacterial test systems, i.e., the Ames reversion test and a liquid DNA-repair test in Escherichia coli. Seventy-five compounds were found to undergo a more or less pronounced decrease of genotoxicity, in at least one of these models, in the presence of rat liver homogenates or in other metabolic systems (up to 40 different preparations, from various sources, for chromium compounds). A number of these deactivable compounds are reported in the literature to yield negative or equivocal results in animal carcinogenicity assays, which may imply the existence of metabolically regulated thresholds in the initiation of cancer. Several examples are provided to support this hypothesis. The in vitro treatment with a pharmacologic agent (N-acetylcysteine) enhanced detoxification mechanisms, either by stimulating enzyme activities promoting glutathione formation in liver homogenates or by reacting itself with direct-acting mutagens and with the genotoxic metabolites of procarcinogens.

Aflatoxin B1↗
PubMed1978

Comparative toxicity of trivalent and hexavalent chromium to rabbits. III. Biochemical and histological changes in testicular tissue.

The administration of trivalent and hexavalent chromium compounds produced inhibition of the activity of succinic dehydrogenase, adenosine triphosphatase and acid phosphattase accompanied by cellular degeneration with complete absence of spermatocytes in the testis of rabbits. The biochemical and histological changes were more marked in the animals treated with the trivalent chromium than those exposed to hexavalent chromium and were progressive with the duration of exposure.

Acid Phosphatase↗
PubMed1983

Differential toxicity and clearance kinetics of chromium(III) or (VI) in mice.

The acute and subacute toxicities of several chromium(III) and chromium(VI) compounds were determined in NZC and (CxO) mice injected i.p. The distal median lethal doses (more than 10 days after treatment) averaged (17.9 +/- 1.8) X 10(-6) g chromium/g body weight regardless of the oxidation state of the chromium compound injected (chromium(III) sulphate may be an exception), but acute toxicity (3 days) was much greater with chromium(VI) compounds. Acid digests of entire male mice that were administered i.p. one-sixth of the distal LD50, either once or repeatedly at weekly intervals, were analysed to determine the whole body persistence and clearance kinetics of chromium. Mice dosed once with chromium(III) retained 6.5 times more chromium at 21 days than mice treated with chromium(VI). When chromium(III) was given at weekly intervals mice accumulated 6 times more chromium by 8 weeks than chromium(VI)-treated mice, though only the latter showed symptoms of chronic toxicity. Whole body chromium concentrations continued to rise with further chromium(III) treatments, but slowly declined with chromium(VI). Analyses of fecal and urinary excretion confirmed most of the urinary chromium clearance occurred soon after injection, and that chromium excretion from chromium(VI)-treated animals was much faster in both urine and feces than from mice given chromium(III). The differential storage and clearance kinetics of chromium(III) and chromium(VI) compounds may be significant in experimental chromium carcinogenesis studies and in the toxicology of chromium in workers exposed industrially to potentially carcinogenic chromium-containing dusts or aerosols.

Animals↗
PubMed1981

Metal interactions in carcinogenesis: enhancement, inhibition.

Metals constitute a fundamentally important part of the total human environment. Since human exposure often involves complex mixtures of metal compounds and, possibly, organic compounds which may be carcinogenic per se, interactions between these compounds may add significantly to human cancer risk. Our present knowledge about these kinds of interactions is very limited. The best investigated area is benzo(a)pyrene (BP)-metal oxide particle interactions in respiratory carcinogenesis in the hamster. Metal oxide particles were also shown to modify the carcinogenic effect of nitrosamines. Several reports describe experiments in which selenium compounds exerted a generally anticarcinogenic and antimutagenic activity. Inorganic arsenic compounds, which are accepted to be carcinogenic in man, have so far been negative in animal experiments except for one recent suggested report. Several authors have, however, suggested that these compounds may act as cocarcinogens due to their inhibition of DNA repair, although animal experiments to demonstrate a cocarcinogenic effect of arsenic compounds have been negative so far, except for one preliminary report. The concentration of zinc in the diet seemed to influence both transplanted tumor growth and the carcinogenicity of several organic compounds, and the possibility of a correlation between dietary zinc and certain cancer forms in man has been suggested. Protection against development of Leydigiomas usually induced by cadmium injection was afforded by simultaneous injection of zinc salts. Nickel carcinogenesis has been reported to be antagonized by manganese, and synergism between Ni and organic carcinogens, e.g. BP, has been demonstrated. There is no firm evidence that lead may be a cocarcinogen, although some limited experimental evidence is available. Oxidizing agents have been demonstrated to increase, and reducing agents to antagonize, the mutagenic effect of chromium compounds in vitro. The content of carcinogenic and other metals in asbestos has been suggested to modify the carcinogenic properties of asbestos. Since much of the information available at present is suggestive, further research on these interactions as well as other possible interactions in metal carcinogenesis is needed. Studies should be made both in well defined in vitro systems and in relevant animal models.

Animals↗
PubMed1980

Mechanisms of chromium toxicity in mammalian cell cultures.

Our observations about the cytotoxic and cytogenetic effects of hexavalent and trivalent chromium compounds in mammalian cells cultured in vitro are reviewed. Additional data concerning the induction of chromosomal aberrations and sister chromatid exchanges, the inhibition of nucleic acid and protein synthesis, the interference with nucleotide metabolism, and the modification of membrane-linked enzyme activity are reported. A possible mechanism of chromium action is proposed.

Animals↗
PubMed1986

DNA-protein crosslinking by heavy metals in Novikoff hepatoma.

Crosslinking of proteins to DNA was studied in live intact Novikoff ascites hepatoma cells exposed in vitro to salts of chromium VI, III, and II, nickel II, cadmium II, and to CoCl2, As2O3, and AlK(SO4)2. DNA-protein complexes were separated by high-speed centrifugation of cells solubilized in buffered 4% sodium dodecyl sulfate and assayed by polyacrylamide gel electrophoresis. Hexavalent chromium compounds formed DNA-protein complexes very efficiently. The trivalent, poorly soluble, cupric chromite was nearly as efficient crosslinker as hexavalent Cr, perhaps because phagocytosis facilitated its entry into the cells. The more basic divalent form produced hardly any crosslinks. Most of the crosslinked proteins were common to all of the chromium salts employed. Nickel salts formed DNA-protein crosslinks less efficiently. Most proteins crosslinked by this metal had a high molecular weight ranging from 94,000 to 200,000. There was little qualitative difference between the crosslinked protein patterns for several various nickel (II) salts. Similar results were obtained for cells incubated with cadmium salts. Most of the proteins crosslinked by cadmium had high molecular weights and were similar to those crosslinked by nickel (II). Relatively weak, but significant, crosslinking was also observed when the Novikoff hepatoma cells were exposed to CoCl2, As2O3, or AlK(SO4)2.

Aluminum↗
PubMed1979

[Chromosome changes induced by industrial chemicals (author's transl)].

Radiation-induced chromosome damage has been widely recognized and intensively studied. Recently, attention is placed on chromosome changes induced by various industrial chemicals. In case of occupational exposure to ionizing radiation, chromosome breaks are characterized as one of the most sensitive biological effects. Chromosome breaks among industrial workers who dealt with benzene, vinyl chloride monomer or styrene have also been reported. Moreover, relationship between chromosome changes and exposure to environmental lead, cadmium and mercury compounds have been studied. Ionizing radiation, benzene and vinyl chloride monomer are known also as industrial carcinogens and attention is now placed on carcinogenicity of clastogens or chromosome breaking agents. In the present paper, our studies on in vitro chromosome breakage induced by benzene and its metabolites as well as cadmium, lead, and chromium compounds are reviewed. Also, inhibition of repair of radiation-induced chromosome breaks by clastogens is reported. Significance of cytogenetic studies in industrial medicine is also discussed.

Adult↗
PubMed1992

Transcriptional inhibition by carcinogenic chromate: relationship to DNA damage.

Hexavalent chromium compounds are carcinogenic to humans, are potent inducers of tumors in experimental animals, and can neoplastically transform cells in culture. In this study, the effects of sodium chromate on the expression of the 78-kDa glucose-regulated protein (GRP78) gene and on general transcription were investigated with respect to the DNA damage induced by this agent. DNA single-strand breaks, DNA-protein cross-links, and chromium-DNA adducts were present in CHO cells immediately after 2 h of treatment with sodium chromate. Subsequently, these types of damage were repaired at different rates. Single-strand breaks were essentially repaired after 8 h. By 24 h posttreatment, no cross-links remained in cells exposed to 30 or 150 microM chromate, although cells treated with the 300-microM concentration still contained cross-links at that time. DNA-chromium adducts remained unrepaired for at least 32 h. The moderate constitutive level of GRP78 mRNA was not affected by chromate. Chromate did, however, suppress induction of this gene by tunicamycin in a concentration-and time-dependent manner. Thirty micromolar sodium chromate (96% survival), which caused the least DNA damage, had no effect on GRP78 induction, general RNA synthesis, or mRNA synthesis. Induction of GRP78 was suppressed immediately and 12 h after treatment with 150 microM chromate (54% survival), although there was a partial recovery of induction at 24 h after treatment, which correlated with the repair of DNA-protein cross-links. In contrast, both total cytoplasmic RNA and mRNA synthesis were suppressed by approximately 60-75% for at least 32 h by 150 microM chromate. At the 300-microM concentration (8% survival), where DNA-protein cross-links persisted beyond 24 h, GRP78 induction was totally suppressed for at least 24 h, while total RNA and mRNA synthesis were suppressed by 80-90% for at least 32 h. Overall, the effects of chromate on GRP78 induction correlated most closely with the presence of DNA-protein cross-links, but suppression of total RNA and mRNA synthesis correlated with the presence of DNA-chromium adducts. These results indicate that chromate exerts differential effects on the induction of the GRP78 gene and on general transcription.

Animals↗
PubMed2003

Effects of hexavalent chromium on the plasma membranes of sensitive and tolerant mutants of Schizosaccharomyces pombe. An EPR study.

The interactions of chromium(VI) with the plasma membranes of chromium-sensitive (chr-51S) and chromium-tolerant (chr1-66T) mutants and their parental strain (6chr(+)) of a Schizosaccharomyces pombe strain were studied by electron paramagnetic resonance (EPR) spectroscopy. 5-doxylstearic acid (5-SASL) and 3-doxylbutyric acid (HO-185) spin probes were used to label the membranes. The order parameter S from the EPR spectra was calculated at different temperatures (0-25 degrees C) in order to characterize the internal dynamics of the membranes. In control experiments, both mutants exhibited differences in structural transitions in the both 5-SASL- and the HO-185-labeled membranes in comparison with their parental strain, suggesting differences in the membrane composition and/or rotational dynamics of these mutants. Addition of K(2)Cr(2)O(7) (225 microM) induced small decreases in the phase transition temperatures of the 5-SASL-labeled membranes of the parental and chromium-sensitive strains. More pronounced effects of the chromium compound on the HO-185-labeled membranes were detected as evidence that the membrane perturbations are mostly localized in the environment of the lipid-water interface.

Cations↗
PubMed1986

Investigation of the potential carcinogenicity of a range of chromium containing materials on rat lung.

Twenty one chromium containing materials were examined for carcinogenic activity in a two year study using an intrabronchial pellet implantation system whereby pellets loaded with test material were surgically implanted into the lower left bronchus of rats. The principal aim of the study was to extend our knowledge of the carcinogenic potential of chromium compounds and, in particular, chromates (Cr6+). A statistically significant incidence of treatment related lung tumours was found with some sparingly soluble chromate materials. All tumours were large keratinizing squamous carcinomas of the left lung, except for a single left lung adenocarcinoma and two left lung anaplastic carcinomas. No bronchial carcinomas (0/100) were seen in the negative control group (blank pellet loaded with cholesterol), whereas bronchial carcinomas (22/48 and 25/100) occurred in the two positive control groups which received pellets loaded with 20-methylcholanthrene and calcium chromate respectively. Among the 20 test materials, only three groups gave statistically significant numbers of bronchial carcinomas. Two of these were groups receiving different samples of strontium chromate which gave 43/99 and 62/99 tumours. The third group, zinc chromate (low solubility), gave 5/100 bronchial carcinomas. A further zinc chromate group (Norge composition) produced 3/100 bronchial carcinomas which was not statistically significant. A few lung tumours were observed in other test groups.

Animals↗